The link between cardiovascular disease (CVD) and metabolic dysfunction-associated steatotic liver disease (MASLD) is well-established at both the epidemiological and pathophysiological levels. Among the common pathophysiological mechanisms involved in the development and progression of both diseases, oxidative stress and inflammation, insulin resistance, lipid metabolism deterioration, hepatokines, and gut dysbiosis along with genetic factors have been recognized to play a pivotal role. Pharmacologic interventions with drugs targeting common modifiable cardiometabolic risk factors, such as T2DM, dyslipidemia, and hypertension, are a reasonable strategy to prevent CVD development and progression of MASLD. Recently, a novel drug for metabolic dysfunction-associated steatohepatitis (MASH), resmetirom, has shown positive effects regarding CVD risk, opening new opportunities for the therapeutic approach of MASLD and CVD. This review provides current knowledge on the epidemiologic association of MASLD to CVD morbidity and mortality and enlightens the possible underlying pathophysiologic mechanisms linking MASLD with CVD. The role of cardiometabolic drugs such as anti-hypertensive drugs, hypolipidemic agents, glucose-lowering medications, acetylsalicylic acid, and the thyroid hormone receptor-beta agonist in the progression of MASLD is also discussed. Metformin failed to prove beneficial effects in MASLD progression. Studies on the administration of thiazolinediones in MASLD suggest effectiveness in improving steatosis, steatohepatitis, and fibrosis, while newer categories of glucose-lowering agents such as GLP-1Ra and SGLT-2i are currently being tested for their efficacy across the whole spectrum of MASLD. Statins alone or in combination with ezetimibe have yielded promising results. The conduction of long-duration, large, high-quality, randomized-controlled trials aiming to assess by biopsy the efficacy of cardiometabolic drugs to reverse MASLD progression is of great importance.

Ischemic stroke (IS) is a severe complication and leading cause of mortality in patients under extracorporeal membrane oxygenation (ECMO). The aim of our narrative review is to summarize the existing evidence and provide a deep examination of the diagnosis and treatment of acute ischemic stroke patients undergoing ECMO support. The incidence rate of ISs is estimated to be between 1 and 8%, while the mortality rate ranges from 44 to 76%, depending on several factors, including ECMO type, duration of support and patient characteristics. Several mechanisms leading to ISs during ECMO have been identified, with thromboembolic events and cerebral hypoperfusion being the most common causes. However, considering that most of the ECMO patients are severely ill or under sedation, stroke symptoms are often underdiagnosed. Multimodal monitoring and daily clinical assessment could be useful preventive techniques. Early recognition of neurological deficits is of paramount importance for prompt therapeutic interventions. All ECMO patients with suspected strokes should immediately receive brain computed tomography (CT) and CT angiography (CTA) for the identification of large vessel occlusion (LVO) and assessment of collateral blood flow. CT perfusion (CTP) can further assist in the detection of viable tissue (penumbra), especially in cases of strokes of unknown onset. Catheter angiography is required to confirm LVO detected on CTA. Intravenous thrombolytic therapy is usually contraindicated in ECMO as most patients are on active anticoagulation treatment. Therefore, mechanical thrombectomy is the preferred treatment option in cases where there is evidence of LVO. The choice of the arterial vascular access used to perform mechanical thrombectomy should be discussed between interventional radiologists and an ECMO team. Anticoagulation management during the acute phase of IS should be individualized after the thromboembolic risk has been carefully balanced against hemorrhagic risk. A multidisciplinary approach is essential for the optimal management of ISs in patients treated with ECMO.

The link between cardiovascular disease (CVD) and non-alcoholic fatty liver disease (NAFLD)/metabolic dysfunction-associated fatty liver disease (MAFLD)/metabolic dys-function-associated steatotic liver disease (MASLD) is well-established at both epidemi-ological and pathophysiological level. Among the common pathophysiological mechanisms involved in the development and progression of both diseases, oxidative stress and inflammation, insulin resistance, lipid metabolism deterioration, gut dysbiosis along with genetic factors have been rec-ognized to play a pivotal role. Pharmacologic interventions with drugs targeting common modifiable cardiometabolic risk factors, such as T2DM, dyslipidemia, and hypertension is a reasonable strategy to prevent CVD development and progression of MASLD. Recently, a novel drug for MASH, resmetirom, has shown positive effects regarding CVD risk, opening new opportunities for the therapeutic approach of NAFLD/MAFLD/MASLD and CVD. This review provides current knowledge on the epidemiologic association of NAFLD/MAFLD/MASLD to CVD morbidity and mortality and enlightens the possible underlying pathophysiologic mechanisms linking NAFLD/MAFLD/MASLD with CVD. It also highlights potential common therapeutic interventions with cardiometabolic drugs such as anti-hypertensive drugs, hypolipidemic agents, glucose-lowering medications, salicylic acid and the thyroid hormone receptor-beta agonist that may improve outcomes of NAFLD/MAFLD/MASLD.